Enterohemorrhagic Escherichia coli (EHEC)

O157:H7

What is the most common, clinical serotype?

Gram-negative

Gram-negative or gram-positive?

Facultative anaerobe

How does it use oxygen?

Two Forms

-non-pathogenic: commensal inhabitant of the intestinal tract
-pathogenic: many different pathotypes/virotypes
*have host specificity; one strain may be pathogenic in one host but non-pathogenic in another (E. coli strains that infect humans don't infect other species)
*some strains also have tissue/organ specificity for where they reside (Ex. ETEC can't infect urogenital tract)

Bacillus (rod-shaped)

What is the morphology?

Characteristics

-outbreaks commonly occur in industrialized countries where food is processed in large factories and distributed across large regions/state lines; not usually found in low-income nations (ETEC more low-income nations)
-referred to as STEC or VTEC (shiga toxin e. coli or verotoxigenic e. coli)
-serotype determined by surface antigen reactivity with antibodies and even surface antigens are unique to each species (ex. several types of O antigens, not just O157)
-surface antigens are PAMPs for PRRs to induce immune response

Flagellin (motile bacteria)

What does the H antigen indicate?

Capsule (EHEC does not have this)

What does the K antigen indicate?

LPS (branched carbohydrate of LPS)

What does the O antigen indicate?

Isolation and Identification of O157:H7

-collection of stool specimens (whole stools, swabs from stool, rectal swabs)
-culture bacteria on Sorbitol-MacConkey (SMAC) agar plates (EHEC doesn't ferment sorbitol unlike other E. coli strains, so plate will remain a brown color with colorless colonies)
-test sorbitol colonies for presence of O157 antigen by latex agglutination
-additional tests for H7 antigen with latex agglutination
-PCR testing for Shiga toxin

EHEC Transmission

-hemolytic uremic syndrome (HUS) typically manifests in children less than 5 years of age and adults 60 and older (weak immune systems)
-majority of infections contracted from contaminated food like meat, vegetables, or fruit(65% of cases)
-person-to-person (fecal-oral route)
-zoonotic contact
-contaminated drinking water
-unknown sources
-gastrointestinal tracts of cows are the most common reservoirs of EHEC

Treatment

-mainly symptom/case monitoring and management
-diarrhea will lead to dehydration so patients must stay hydrated (IV isotonic fluids)
-do not use antimotility drugs like antidiuretics or Pepto because they will keep you from shedding the bacteria if you are not using the bathroom
-monitor RBC counts because EHEC produces a hemolysin that can destroy these cells, leading to hemolytic anemia (give RBC transfusions when necessary)
-watch out for thrombocytopenia and acute kidney injury (platelet transfusions and hydration/electrolyte management or dialysis for kidneys)
-usually clears on its own

Virulence Factors

-Shiga toxin, attacks kidney cells and causes HUS
-produce hemolysins
-low acid-resistance
-low infectious dose (about 10)
-T3SS to secrete Shiga toxin
-adhesive pili
-non-pilus adhesions

Pathogenicity Islands

discrete segments of DNA that encode virulence genes such as genes or type III secretion systems and associated regulators

Shiga Toxin

-AB5 toxin (a=active polypeptide; b=binding polypeptide)
-only gets released when outer membrane of bacteria is disrupted/broken down
-B toxin binds bacterium to a host cell and triggers the cell to endocytose the bacterium
-A toxin targets the 28S ribosomal RNA to remove purine nucleotide and ultimately kill ribosome

Why No Antibiotics for EHEC?

-phage proteins in the bacterium kick into the lytic cycle when antibiotics are given because they sense danger/attack
-this makes the phage genome replicate and create thousands of copies of the toxin genes within bacterium; leads to amplified infection for patient

Pedestal Formation

-T3SS release effector proteins (called Tir) that force pedestals to grow on the surfaces of host cells
-actin monomers are polymerized and create long strands that push the host cell membrane up
-pedestals interfere with availability of actin in phagocytes which messes up the process of phagocytosis; phagocytosis is actin-dependent
-pedestals are motile so bacteria can surf on surface of hsot cells to spread to others